Among cancers, breast cancer is a cancer that women suffer from most frequently. Along with westernization of diets and aging of population, the number of patients has continued to increase in recent years.
As therapeutic techniques for breast cancer, clinically, surgical treatments such as mammary gland resection, chemotherapy using anticancer drugs, and radiation therapy have been widely used.
The mammary epithelium proliferates by the action of estrogen which is a female hormone, and thus also in breast cancer of estrogen receptor positive, the proliferation is stimulated in an estrogen dependent manner. Therefore, in general, for tumors of estrogen receptor positive or progesterone receptor positive which are expected to be estrogen sensitive, hormone therapy is performed using antiestrogens or aromatase suppressants that cause inhibition of estrogen production. Moreover, hormone therapy is performed for advanced breast cancer as well.
Meanwhile, even in breast cancer to which hormone therapy is initially recognized to be effective, there is a problem with acquisition of resistance during the course of therapy (see, for example, NPL 1). Conceivable causes of this include: excessive expression or activation of an estrogen receptor that can occur after an estrogen depleted state; and enhancement of the action of molecules that are originally estrogen receptor targeting factors and cause cancerous proliferation, even after acquisition of resistance.
Therefore, therapy for targeting molecules downstream of an estrogen signal, especially factors causing cancerous proliferation, is expected as an effective therapeutic technique in place of the existing hormone therapy.
However, the molecular mechanism of resistance to hormone therapy has not yet been revealed in detail, and thus any sufficient therapeutic method for breast cancer after acquisition of resistance and therapy-resistant breast cancer has not yet been developed.
In addition, for tumor that is growth factor HER2 molecule positive in breast cancer of estrogen receptor negative, molecular targeted therapy is also performed including monoclonal antibody therapy against HER2. However, at present, there is no effective therapeutic method for breast cancer of estrogen receptor negative, progesterone receptor negative, and HER2 negative.
As described above, there is a limit in the existing therapeutic techniques, and strong demand has currently arisen for prompt development of a method for suppressing breast cancer including refractory breast cancer to which the existing breast cancer therapeutic techniques are not recognized to be effective.
Also, for other cancers than breast cancer, strong demand has currently arisen for prompt development of a method for suppressing cancer.